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{{Short description|Inability to distinguish sounds}}
'''Auditory agnosia''' is a form of [[agnosia]] that manifests itself primarily in the inability to recognize or differentiate between [[sound]]s. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered.<ref>{{cite book |last1=Slevc |first1=L.R. |last2=Shell |first2=A.R. |chapter=Auditory agnosia |title=The Human Auditory System - Fundamental Organization and Clinical Disorders |series=Handbook of Clinical Neurology |date=2015 |volume=129 |pages=573–587 |doi=10.1016/B978-0-444-62630-1.00032-9 |pmid=25726291 |isbn=9780444626301 |url=https://pubmed.ncbi.nlm.nih.gov/25726291/ |access-date=9 December 2021}}</ref> It is caused by bilateral damage to the [[anterior superior temporal gyrus]], which is part of the auditory pathway responsible for [[sound recognition]], the auditory [[Two-streams hypothesis#Ventral stream|"what" pathway]].<ref name=":9">{{cite journal | vauthors = Poliva O, Bestelmeyer PE, Hall M, Bultitude JH, Koller K, Rafal RD | title = Functional Mapping of the Human Auditory Cortex: fMRI Investigation of a Patient with Auditory Agnosia from Trauma to the Inferior Colliculus | journal = Cognitive and Behavioral Neurology | volume = 28 | issue = 3 | pages = 160–80 | date = September 2015 | pmid = 26413744 | doi = 10.1097/WNN.0000000000000072 | s2cid = 913296 | url = http://opus.bath.ac.uk/48370/1/Poliva_Rafal_Auditory_Agnosia_CBN_v28n3_Sept2015.pdf }}</ref>

Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it ''was'' a lion creating the noise.<ref name="Martin 2006">{{Cite book | vauthors = Martin GN | title = Human neuropsychology | date = 2006 | publisher = Pearson/Prentice Hall | location = Harlow, England; New York | isbn = 978-0-13-197452-4 | oclc = 61692682 }}</ref> All auditory agnosia patients read lips in order to enhance the speech comprehension.<ref name=":10">{{cite journal | vauthors = Buchman AS, Garron DC, Trost-Cardamone JE, Wichter MD, Schwartz M | title = Word deafness: one hundred years later | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 49 | issue = 5 | pages = 489–99 | date = May 1986 | pmid = 2423648 | pmc = 1028802 | doi = 10.1136/jnnp.49.5.489 }}</ref>

It is yet unclear whether auditory agnosia (also called general auditory agnosia) is a combination of milder disorders, such [[auditory verbal agnosia]] (pure word deafness), non-verbal auditory agnosia, [[amusia]] and word-meaning deafness, or a mild case of the more severe disorder, cerebral deafness. Typically, a person with auditory agnosia would be incapable of comprehending spoken language as well as environmental sounds. Some may say that the milder disorders are how auditory agnosia occurs. There are few cases where a person may not be able to understand spoken language. This is called verbal auditory agnosia or pure word deafness.<ref>{{cite journal |last1=Buchtel |first1=H.A. |title=Auditory Agnosia |journal=Encyclopedia of the Human Brain |date=2002 |pages=285–287 |doi=10.1016/B0-12-227210-2/00011-X |isbn=9780122272103 |url=https://www.sciencedirect.com/science/article/pii/B012227210200011X |access-date=9 December 2021}}</ref> Nonverbal auditory agnosia is diagnosed when a person’s understanding of environmental sounds is inhibited. Combined, these two disorders portray auditory agnosia.<ref>{{cite journal |last1=Simons |first1=J.S. |last2=Ralph |first2=M.A.L. |title=Previous Cases: The Auditory Agnosias |journal=Neurocase |date=1999 |volume=5 |pages=379–406 |doi=10.1093/neucas/5.5.379 |url=http://www.memlab.psychol.cam.ac.uk/pubs/Simons1999%20Neurocase.pdf |access-date=9 December 2021}}</ref> The blurriness between the combination of these disorders may lead to discrepancies in reporting. {{As of|2014|}}, 203 patients with auditory perceptual deficits due to CNS damage were reported in the medical literature, of which 183 diagnosed with general auditory agnosia or word deafness, 34 with cerebral deafness, 51 with non-verbal auditory agnosia-amusia and 8 word meaning deafness (for a list of patients see<ref name=":0">{{cite thesis | vauthors = Poliva O | date = 2014 | title = Neuroanatomical and perceptual deficits in auditory agnosia: a study of an auditory agnosia patient with inferior colliculus damage. | degree = Ph.D. | publisher = Prifysgol Bangor University | url = https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.665578 | pages = 67–74 }}</ref>).

== History ==
A relationship between hearing and the brain was first documented by Ambroise Paré, a 16th century battlefield doctor, who associated parietal lobe damage with acquired deafness (reported in Henschen, 1918<ref>{{Cite journal| vauthors = Henschen SE |date= January 1918 |title=On the hearing Sphere|journal=Acta Oto-Laryngologica|volume=1|issue=1|pages=423–485|doi=10.3109/00016481809122009|issn=0001-6489|url= https://zenodo.org/record/2434325 }}</ref>). Systematic research into the manner in which the brain processes sounds, however, only began toward the end of the 19th century. In 1874, Wernicke<ref>{{cite book|last=Wernicke|first=Carl |chapter=Der aphasische Symptomenkomplex | name-list-style = vanc |date=1974|pages=1–70|publisher=Springer Berlin Heidelberg|isbn=978-3-540-06905-8|doi=10.1007/978-3-642-65950-8_1}}</ref> was the first to ascribe to a brain region a role in auditory perception. Wernicke proposed that the impaired perception of language in his patients was due to losing the ability to register sound frequencies that are specific to spoken words (he also suggested that other aphasic symptoms, such as speaking, reading and writing errors occur because these speech specific frequencies are required for feedback). Wernicke localized the perception of spoken words to the posterior half of the left STG (superior temporal gyrus). Wernicke also distinguished between patients with auditory agnosia (which he labels as receptive aphasia) with patients who cannot detect sound at any frequency (which he labels as cortical deafness).<ref name=":1">{{cite journal | vauthors = Wernicke C, Friedlander C | title = Ein Fall von Taubheit in folge von doppelseiteger Laesion des Schläfenlappens | journal = Fortschr. Med. | date = 1883 | volume = 1 | pages = 177–185 }}</ref>

In 1877, Kussmaul was the first to report auditory agnosia in a patient with intact hearing, speaking, and reading-writing abilities. This case-study led Kussmaul to propose of distinction between the word perception deficit and Wernicke's sensory aphasia. He coined the former disorder as "word deafness". Kussmaul also localized this disorder to the left STG. Wernicke interpreted Kussmaul's case as an incomplete variant of his sensory aphasia.<ref name=":1" />

In 1885,<ref name=":2">{{Cite journal| vauthors = Lichteim L | date = January 1885 | title=On Aphasia |journal=Brain |volume=7 |issue=4 |pages=433–484 |doi=10.1093/brain/7.4.433 }}</ref> Lichtheim also reported of an auditory agnosia patient. This patient, in addition to word deafness, was impaired at recognizing environmental sounds and melodies. Based on this case study, as well as other aphasic patients, Lichtheim proposed that the language reception center receives afferents from upstream auditory and visual word recognition centers, and that damage to these regions results in word deafness or word blindness (i.e., alexia), respectively. Because the lesion of Lichtheim's auditory agnosia patient was sub-cortical deep to the posterior STG (superior temporal gyrus), Lichtheim renamed auditory agnosia as "sub-cortical speech deafness".

The language model proposed by Wernicke and Lichtheim wasn't accepted at first. For example, in 1897 Bastian<ref>{{Cite journal |last=Bastian |first= H. Charlton | name-list-style = vanc |date= April 1897 |title= The Lumleian Lectures on some problems in connection with aphasia and other speech defects: Lecture 1 |journal=The Lancet|volume=149|issue=3843|pages=1131–1137|doi=10.1016/s0140-6736(01)95713-7|issn=0140-6736|url= https://zenodo.org/record/1672117 |hdl=11858/00-001M-0000-002A-5068-C|hdl-access=free}}</ref> argued that, because aphasic patients can repeat single words, their deficit is in the extraction of meaning from words. He attributed both aphasia and auditory agnosia to damage in Lichtheim's auditory word center. He hypothesized that aphasia is the outcome of partial damage to the left auditory word center, whereas auditory agnosia is the result of complete damage to the same area. Bastian localized the auditory word center to the posterior MTG (middle temporal gyrus).

Other opponents to the Wernicke-Lichtheim model were Sigmund Freud and Carl Freund. Freud<ref name=":3">{{cite book | vauthors = Freud S | title = Zur Auffassung der Aphasien | url = https://archive.org/details/ZurAuffassungDerAphasien.EineKritischeStudie | location = Vienna | publisher = Franz Deuticke | date = 1891 }}</ref> (1891) suspected that the auditory deficits in aphasic patients was due to a secondary lesion to cochlea. This assertion was confirmed by Freund<ref>{{cite book | vauthors = Freund CS | title = Labyrinthtaubheit und Sprachtaubheit | url = https://archive.org/details/labyrinthtaubhe00freugoog | location = Wiesbaden | publisher = Bergmann | date = 1895 }}</ref> (1895), who reported two auditory agnosia patients with cochlear damage (although in a later autopsy, Freund reported also the presence of a tumor in the left STG in one of these patients). This argument, however, was refuted by Bonvicini<ref>{{cite journal | vauthors = Bonvicini G | title = Über subcorticale sensorische Aphasie. | journal = Jahrbücher für Psychiatrie | date = 1905 | volume = 26 | pages = 126–229 }}</ref> (1905), who measured the hearing of an auditory agnosia patient with tuning forks, and confirmed intact pure tone perception. Similarly, Barrett's aphasic patient,<ref>{{cite journal |last=Barrett |first=Albert M. | name-list-style = vanc |date= February 1910 |title=A case of pure word-deafness with autopsy |journal=The Journal of Nervous and Mental Disease |volume=37 |issue=2 |pages=73–92 |doi=10.1097/00005053-191002000-00001 |s2cid=148432237 |url=https://zenodo.org/record/1549109 }}</ref> who was incapable of comprehending speech, had intact hearing thresholds when examined with tuning forks and with a Galton whistle. The most adverse opponent to the model of Wernicke and Lichtheim was Marie<ref>{{cite book | vauthors = Marie P | chapter = What to think about subcortical aphasias (pure aphasias) | series = Semaine Medicale 26 | pages = 493–500 | veditors = Cole MR, Cole M | title = Pierre Marie's Papers on Speech Disorders | location = New York | publisher = Hafner | date = 1906 }}</ref> (1906), who argued that all aphasic symptoms manifest because of a single lesion to the language reception center, and that other symptoms such as auditory disturbances or paraphasia are expressed because the lesion encompasses also sub-cortical motor or sensory regions.

In the following years, increasing number of clinical reports validated the view that the right and left auditory cortices project to a language reception center located in the posterior half of the left STG, and thus established the Wernicke-Lichtheim model. This view was also consolidated by Geschwind<ref>{{cite journal | vauthors = Geschwind N | title = Disconnexion syndromes in animals and man. I | journal = Brain | volume = 88 | issue = 2 | pages = 237–94 | date = June 1965 | pmid = 5318481 | doi = 10.1093/brain/88.2.237 | doi-access = free }}</ref> (1965) who reported that, in humans, the left planum temporale is larger in the left hemisphere than on the right. Geschwind interpreted this asymmetry as anatomical verification for the role of left posterior STG in the perception of language.

The Wernicke-Lichtheim-Geschwind model persisted throughout the 20th century. However, with the advent of MRI and its usage for lesion mapping, it was shown that this model is based on incorrect correlation between symptoms and lesions.<ref>{{cite journal | vauthors = DeWitt I, Rauschecker JP | title = Phoneme and word recognition in the auditory ventral stream | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 8 | pages = E505–14 | date = February 2012 | pmid = 22308358 | pmc = 3286918 | doi = 10.1073/pnas.1113427109 | bibcode = 2012PNAS..109E.505D | doi-access = free }}</ref><ref>{{cite journal | vauthors = Mesulam MM, Thompson CK, Weintraub S, Rogalski EJ | title = The Wernicke conundrum and the anatomy of language comprehension in primary progressive aphasia | journal = Brain | volume = 138 | issue = Pt 8 | pages = 2423–37 | date = August 2015 | pmid = 26112340 | pmc = 4805066 | doi = 10.1093/brain/awv154 }}</ref><ref>{{cite journal | vauthors = [[David Poeppel|Poeppel D]], [[Karen Emmorey|Emmorey K]], Hickok G, [[Liina Pylkkänen|Pylkkänen L]] | title = Towards a new neurobiology of language | journal = The Journal of Neuroscience | volume = 32 | issue = 41 | pages = 14125–31 | date = October 2012 | pmid = 23055482 | pmc = 3495005 | doi = 10.1523/jneurosci.3244-12.2012 }}</ref> Although this model is considered outdated, it is still widely mentioned in Psychology and medical textbooks, and consequently in medical reports of auditory agnosia patients. As will be mentioned below, based on cumulative evidence the process of sound recognition was recently shifted to the left and right anterior auditory cortices, instead of the left posterior auditory cortex.

== Related disorders ==
After auditory agnosia was first discovered, subsequent patients were diagnosed with different types of hearing impairments. In some reports, the deficit was restricted to spoken words, environmental sounds or music. In one case study, each of the three sound types (music, environmental sounds, speech) was also shown to recover independently (Mendez and Geehan, 1988-case 2<ref>{{cite journal | vauthors = Mendez MF, Geehan GR | title = Cortical auditory disorders: clinical and psychoacoustic features | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 51 | issue = 1 | pages = 1–9 | date = January 1988 | pmid = 2450968 | doi = 10.1136/jnnp.51.1.1 | pmc = 1032706 }}</ref>). It is yet unclear whether general auditory agnosia is a combination of milder auditory disorders, or whether the source of this disorder is at an earlier auditory processing stage.

=== Cerebral deafness ===
Cerebral deafness (also known as cortical deafness or central deafness) is a disorder characterized by complete deafness that is the result of damage to the central nervous system. The primary distinction between auditory agnosia and cerebral deafness is the ability to detect pure tones, as measured with pure tone audiometry. Using this test, auditory agnosia patients were often reported<ref>{{Citation|last=Vignolo|first=Luigi A. | name-list-style = vanc |chapter=Auditory Agnosia: A Review and Report of Recent Evidence |title=Brain & Behavior |date=2017-07-12 |pages=172–208 |publisher=Routledge |isbn=978-1-315-08203-5 |doi=10.4324/9781315082035-8 |doi-access=free }}</ref><ref name=":4">{{cite journal | vauthors = Tanaka Y, Kamo T, Yoshida M, Yamadori A | title = 'So-called' cortical deafness. Clinical, neurophysiological and radiological observations | journal = Brain | volume = 114 ( Pt 6) | issue = 6 | pages = 2385–401 | date = December 1991 | pmid = 1782522 | doi = 10.1093/brain/114.6.2385 }}</ref> capable of detecting pure tones almost as good as healthy individuals, whereas cerebral deafness patients found this task almost impossible or they required very loud presentations of sounds (above 100&nbsp;dB). In all reported cases, cerebral deafness was associated with bilateral temporal lobe lesions. A study<ref name=":4" /> that compared the lesions of two cerebral deafness patients to an auditory agnosia patient concluded that cerebral deafness is the result of complete de-afferentation of the auditory cortices, whereas in auditory agnosia some thalamo-cortical fibers are spared. In most cases the disorder is transient and the symptoms mitigate into auditory agnosia (although chronic cases were reported<ref>{{cite journal | vauthors = Polster MR, Rose SB | title = Disorders of auditory processing: evidence for modularity in audition | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 34 | issue = 1 | pages = 47–65 | date = February 1998 | pmid = 9533993 | doi = 10.1016/s0010-9452(08)70736-6 | s2cid = 2717085 }}</ref>). Similarly, a monkey study<ref>{{cite journal | vauthors = Heffner HE, Heffner RS | title = Effect of bilateral auditory cortex lesions on absolute thresholds in Japanese macaques | journal = Journal of Neurophysiology | volume = 64 | issue = 1 | pages = 191–205 | date = July 1990 | pmid = 2388065 | doi = 10.1152/jn.1990.64.1.191 }}</ref> that ablated both auditory cortices of monkeys reported of deafness that lasted 1 week in all cases, and that was gradually mitigated into auditory agnosia in a period of 3–7 weeks.

=== Pure word deafness ===
Since the early days of aphasia research, the relationship between auditory agnosia and [[speech perception]] has been debated. Lichtheim<ref name=":2" /> (1885) proposed that auditory agnosia is the result of damage to a brain area dedicated to the perception of spoken words, and consequently renamed this disorder from 'word deafness' to 'pure word deafness'. The description of word deafness as being exclusively for words was adopted by the scientific community despite the patient reported by Lichtheim's who also had more general auditory deficits. Some researchers who surveyed the literature, however, argued against labeling this disorder as pure word deafness on the account that all patients reported impaired at perceiving spoken words were also noted with other auditory deficits or aphasic symptoms.<ref>{{Cite journal| vauthors = Head H |date=1920|title=Aphasia and kindred disorders of speech|journal=Brain|volume=43|issue=2|pages=87–165|doi=10.1093/brain/43.2.87 |hdl=11858/00-001M-0000-002B-9E28-0|hdl-access=free}}</ref><ref name=":10" /> In one review of the literature, Ulrich<ref name=":5">{{cite journal | vauthors = Ulrich G | title = Interhemispheric functional relationships in auditory agnosia. An analysis of the preconditions and a conceptual model | journal = Brain and Language | volume = 5 | issue = 3 | pages = 286–300 | date = May 1978 | pmid = 656899 | doi = 10.1016/0093-934x(78)90027-5 | s2cid = 33841186 }}</ref> (1978) presented evidence for separation of word deafness from more general auditory agnosia, and suggested naming this disorder "linguistic auditory agnosia" (this name was later rephrased into "verbal auditory agnosia"<ref>{{cite journal | vauthors = Wang E, Peach RK, Xu Y, Schneck M, Manry C | title = Perception of dynamic acoustic patterns by an individual with unilateral verbal auditory agnosia | journal = Brain and Language | volume = 73 | issue = 3 | pages = 442–55 | date = July 2000 | pmid = 10860565 | doi = 10.1006/brln.2000.2319 | s2cid = 18865116 }}</ref>). To contrast this disorder with auditory agnosia in which speech repetition is intact (word meaning deafness), the name "word sound deafness"<ref>{{Cite journal| vauthors = Kohn SE, Friedman RB | title = Word-meaning deafness: A phonological-semantic dissociation. | journal = Cognitive Neuropsychology | date = August 1986 | volume = 3 | issue = 3 | pages = 291–308 | doi = 10.1080/02643298608253361 }}</ref> and "phonemic deafness"<ref name=":12">{{cite book | vauthors = Kleist K | chapter = Phonemic Deafness (So-Called Pure Word Deafness). | title = Sensory Aphasia and Amusia | location = New York | publisher = Pergamon Press | date = 1962 | pages = 28–41 }}</ref> (Kleist, 1962) were also proposed. Although some researchers argued against the purity of word deafness, some anecdotal cases with exclusive impaired perception of speech were documented.<ref>{{Cite journal| vauthors = Mills CK |date=1891|title=On the localisation of the auditory centre|journal=Brain|volume=14|issue=4|pages=465–472|doi=10.1093/brain/14.4.465|issn=0006-8950|url=https://zenodo.org/record/2032930|doi-access=free}}</ref><ref>{{Cite journal|last=Ziehl|first=Franz | name-list-style = vanc |date= March 1896 |title=Ueber einen Fall von Worttaubheit und das Lichtheim'sche Krankheitsbild der subcorticalen sensorischen Aphasie|journal=Deutsche Zeitschrift für Nervenheilkunde|volume=8-8|issue=3–4|pages=259–307|doi=10.1007/bf01666315|s2cid=37283541 |issn=0340-5354|url=https://zenodo.org/record/1562654 }}</ref><ref>{{cite journal | vauthors = Hemphill RE, Stengel E | title = a study on pure word-deafness | journal = Journal of Neurology and Psychiatry | volume = 3 | issue = 3 | pages = 251–62 | date = July 1940 | pmid = 21610977 | pmc = 1088185 | doi = 10.1136/jnnp.3.3.251 }}</ref><ref>{{cite journal | vauthors = Klein R, Harper J | title = The problem of agnosia in the light of a case of pure word deafness | journal = The Journal of Mental Science | volume = 102 | issue = 426 | pages = 112–20 | date = January 1956 | pmid = 13307190 | doi = 10.1192/bjp.102.426.112 }}</ref><ref>{{cite journal | vauthors = Saffran EM, Marin OS, Yeni-Komshian GH | title = An analysis of speech perception in word deafness | journal = Brain and Language | volume = 3 | issue = 2 | pages = 209–28 | date = April 1976 | pmid = 938928 | doi = 10.1016/0093-934x(76)90018-3 | s2cid = 12334367 }}</ref><ref>{{cite journal | vauthors = Yaqub BA, Gascon GG, Al-Nosha M, Whitaker H | title = Pure word deafness (acquired verbal auditory agnosia) in an Arabic speaking patient | journal = Brain | volume = 111 ( Pt 2) | issue = 2 | pages = 457–66 | date = April 1988 | pmid = 3378145 | doi = 10.1093/brain/111.2.457 }}</ref><ref>{{cite journal | vauthors = Takahashi N, Kawamura M, Shinotou H, Hirayama K, Kaga K, Shindo M | title = Pure word deafness due to left hemisphere damage | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 28 | issue = 2 | pages = 295–303 | date = June 1992 | pmid = 1499314 | doi = 10.1016/s0010-9452(13)80056-1 | s2cid = 4488260 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Tanaka Y, Yamadori A, Mori E | title = Pure word deafness following bilateral lesions. A psychophysical analysis | journal = Brain | volume = 110 ( Pt 2) | issue = 2 | pages = 381–403 | date = April 1987 | pmid = 3567528 | doi = 10.1093/brain/110.2.381 }}</ref><ref>{{cite journal | vauthors = Wolmetz M, Poeppel D, Rapp B | title = What does the right hemisphere know about phoneme categories? | journal = Journal of Cognitive Neuroscience | volume = 23 | issue = 3 | pages = 552–69 | date = March 2011 | pmid = 20350179 | pmc = 4471482 | doi = 10.1162/jocn.2010.21495 }}</ref>{{citation overkill|date=August 2021}} On several occasions, patients were reported to gradually transition from pure word deafness to general auditory agnosia/cerebral deafness<ref>{{cite journal | vauthors = Iizuka O, Suzuki K, Endo K, Fujii T, Mori E | title = Pure word deafness and pure anarthria in a patient with frontotemporal dementia | journal = European Journal of Neurology | volume = 14 | issue = 4 | pages = 473–5 | date = April 2007 | pmid = 17389003 | doi = 10.1111/j.1468-1331.2007.01671.x | s2cid = 45767094 }}</ref><ref name="pmid12735933">{{cite journal | vauthors = Szirmai I, Farsang M, Csüri M | title = Cortical auditory disorder caused by bilateral strategic cerebral bleedings. Analysis of two cases | journal = Brain and Language | volume = 85 | issue = 2 | pages = 159–65 | date = May 2003 | pmid = 12735933 | doi = 10.1016/s0093-934x(02)00597-7 | s2cid = 42467221 }}</ref><ref name=":6">{{cite journal | vauthors = Pinard M, Chertkow H, Black S, Peretz I | title = A case study of pure word deafness: modularity in auditory processing? | journal = Neurocase | volume = 8 | issue = 1–2 | pages = 40–55 | date = February 2002 | pmid = 11997484 | doi = 10.1093/neucas/8.1.40 | s2cid = 38623636 }}</ref> or recovery from general auditory agnosia/cerebral deafness to pure word deafness.<ref>{{cite journal | vauthors = Goldstein MN, Brown M, Hollander J | title = Auditory agnosia and cortical deafness: analysis of a case with three-year followup | journal = Brain and Language | volume = 2 | issue = 3 | pages = 324–32 | date = July 1975 | pmid = 1182499 | doi = 10.1016/s0093-934x(75)80073-3 | s2cid = 1337350 }}</ref><ref>{{cite journal | vauthors = Zhu RJ, Lv ZS, Shan CL, Xu MW, Luo BY | title = Pure word deafness associated with extrapontine myelinolysis | journal = Journal of Zhejiang University Science B | volume = 11 | issue = 11 | pages = 842–7 | date = November 2010 | pmid = 21043052 | pmc = 2970893 | doi = 10.1631/jzus.b1000200 }}</ref>

In a review of the auditory agnosia literature, Phillips and Farmer<ref>{{cite journal | vauthors = Phillips DP, Farmer ME | title = Acquired word deafness, and the temporal grain of sound representation in the primary auditory cortex | journal = Behavioural Brain Research | volume = 40 | issue = 2 | pages = 85–94 | date = November 1990 | pmid = 2285476 | doi = 10.1016/0166-4328(90)90001-u | s2cid = 9626294 }}</ref> showed that patients with word deafness are impaired in their ability to discriminate gaps between click sounds as long as 15-50 milliseconds, which is consistent with the duration of phonemes. They also showed that patients with general auditory agnosia are impaired in their ability to discriminate gaps between click sounds as long as 100–300 milliseconds. The authors further showed that word deafness patients liken their auditory experience to hearing foreign language, whereas general auditory agnosia described speech as incomprehensible noise. Based on these findings, and because both word deafness and general auditory agnosia patients were reported to have very similar neuroanatomical damage (bilateral damage to the auditory cortices), the authors concluded that word deafness and general auditory agnosia is the same disorder, but with a different degree of severity.

Pinard et al<ref name=":6" /> also suggested that pure word deafness and general auditory agnosia represent different degrees of the same disorder. They suggested that environmental sounds are spared in the mild cases because they are easier to perceive than speech parts. They argued that environmental sounds are more distinct than speech sounds because they are more varied in their duration and loudness. They also proposed that environmental sounds are easier to perceive because they are composed of a repetitive pattern (e.g., the bark of a dog or the siren of the ambulance).

Auerbach et al<ref>{{cite journal | vauthors = Auerbach SH, Allard T, Naeser M, Alexander MP, Albert ML | title = Pure word deafness: analysis of a case with bilateral lesions and a defect at the prephonemic level. | journal = Brain | date = June 1982 | volume = 105 | issue = 2 | pages = 271–300 | doi=10.1093/brain/105.2.271 | pmid = 7082991 }}</ref> considered word deafness and general auditory agnosia as two separate disorders, and labelled general auditory agnosia as pre-phonemic auditory agnosia and word deafness as post-phonemic auditory agnosia. They suggested that pre-phonemic auditory agnosia manifests because of general damage to the auditory cortex of both hemispheres, and that post-phonemic auditory agnosia manifests because of damage to a spoken word recognition center in the left hemisphere. Recent evidence, possibly verified Auerbach hypothesis, since an epileptic patient who undergone electro-stimulation to the anterior superior temporal gyrus was demonstrated a transient loss of speech comprehension, but with intact perception of environmental sounds and music.<ref>{{cite journal | vauthors = Matsumoto R, Imamura H, Inouchi M, Nakagawa T, Yokoyama Y, Matsuhashi M, Mikuni N, Miyamoto S, Fukuyama H, Takahashi R, Ikeda A | title = Left anterior temporal cortex actively engages in speech perception: A direct cortical stimulation study | journal = Neuropsychologia | volume = 49 | issue = 5 | pages = 1350–1354 | date = April 2011 | pmid = 21251921 | doi = 10.1016/j.neuropsychologia.2011.01.023 | hdl = 2433/141342 | s2cid = 1831334 | hdl-access = free }}</ref>

=== Non-verbal auditory agnosia ===
The term auditory agnosia was originally coined by Freud<ref name=":3" /> (1891) to describe patients with selective impairment of environmental sounds. In a review of the auditory agnosia literature, Ulrich<ref name=":5" /> re-named this disorder as non-verbal auditory agnosia (although sound auditory agnosia and environmental sound auditory agnosia are also commonly used). This disorder is very rare and only 18 cases have been documented.<ref name=":0" /> In contradiction to pure word deafness and general auditory agnosia, this disorder is likely under-diagnosed because patients are often not aware of their disorder, and thus don't seek medical intervention.<ref name="Saygin AP 2009">{{cite journal | vauthors = Saygin AP, Leech R, Dick F | title = Nonverbal auditory agnosia with lesion to Wernicke's area | journal = Neuropsychologia | volume = 48 | issue = 1 | pages = 107–13 | date = January 2010 | pmid = 19698727 | pmc = 2794980 | doi = 10.1016/j.neuropsychologia.2009.08.015 }}</ref><ref>{{cite journal | vauthors = Vignolo LA | title = Music agnosia and auditory agnosia. Dissociations in stroke patients | journal = Annals of the New York Academy of Sciences | volume = 999 | issue = 1 | pages = 50–7 | date = November 2003 | pmid = 14681117 | doi = 10.1196/annals.1284.005 | bibcode = 2003NYASA.999...50V | s2cid = 145136859 }}</ref><ref name="pmid15199735">{{cite journal | vauthors = Yamamoto T, Kikuchi T, Nagae J, Ogata K, Ogawa M, Kawai M | title = [Dysprosody associated with environmental auditory sound agnosia in right temporal lobe hypoperfusion—a case report] | language = ja | journal = Rinsho Shinkeigaku = Clinical Neurology | volume = 44 | issue = 1 | pages = 28–33 | date = January 2004 | pmid = 15199735 }}</ref>

Throughout the 20th century, all reported non-verbal auditory agnosia patients had bilateral or right temporal lobe damage. For this reason, the right hemisphere was traditionally attributed with the perception of environmental sounds. However, Tanaka et al<ref>{{cite journal | vauthors = Tanaka Y, Nakano I, Obayashi T | title = Environmental sound recognition after unilateral subcortical lesions | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 38 | issue = 1 | pages = 69–76 | date = February 2002 | pmid = 11999335 | doi = 10.1016/s0010-9452(08)70639-7 | s2cid = 4478056 }}</ref> reported 8 patients with non-verbal auditory agnosia, 4 with right hemisphere lesions and 4 with left hemisphere lesions. Saygin<ref name="Saygin AP 2009"/> et al also reported a patient with damage to the left auditory cortex.

The underlying deficit in non-verbal auditory agnosia appears to be varied. Several patients were characterized by impaired discrimination of pitch<ref>{{cite journal | vauthors = Johannes S, Jöbges ME, Dengler R, Münte TF | title = Cortical auditory disorders: a case of non-verbal disturbances assessed with event-related brain potentials | journal = Behavioural Neurology | volume = 11 | issue = 1 | pages = 55–73 | date = 1998 | pmid = 11568403 | doi = 10.1155/1998/190715 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Habib M, Daquin G, Milandre L, Royere ML, Rey M, Lanteri A, Salamon G, Khalil R | title = Mutism and auditory agnosia due to bilateral insular damage--role of the insula in human communication | journal = Neuropsychologia | volume = 33 | issue = 3 | pages = 327–39 | date = March 1995 | pmid = 7791999 | doi = 10.1016/0028-3932(94)00108-2 | s2cid = 12592266 }}</ref><ref>{{cite journal | vauthors = Spreen O, Benton AL, Fincham RW | journal = Archives of Neurology | volume = 13 | issue = 1 | pages = 84–92 | date = July 1965 | pmid = 14314279 | doi = 10.1001/archneur.1965.00470010088012 | title = Auditory Agnosia Without Aphasia }}</ref> whereas others reported with impaired discrimination of timbre and rhythm<ref name=":7">{{cite journal | vauthors = Fujii T, Fukatsu R, Watabe S, Ohnuma A, Teramura K, Kimura I, Saso S, Kogure K | title = Auditory sound agnosia without aphasia following a right temporal lobe lesion | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 26 | issue = 2 | pages = 263–8 | date = June 1990 | pmid = 2082956 | doi = 10.1016/s0010-9452(13)80355-3 | s2cid = 4478913 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Mazzucchi A, Marchini C, Budai R, Parma M | title = A case of receptive amusia with prominent timbre perception defect | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 45 | issue = 7 | pages = 644–7 | date = July 1982 | pmid = 7119832 | pmc = 491481 | doi = 10.1136/jnnp.45.7.644 }}</ref><ref>{{cite journal | vauthors = Eustache F, Lechevalier B, Viader F, Lambert J | title = Identification and discrimination disorders in auditory perception: a report on two cases | journal = Neuropsychologia | volume = 28 | issue = 3 | pages = 257–70 | date = January 1990 | pmid = 2325838 | doi = 10.1016/0028-3932(90)90019-k | s2cid = 20121045 }}</ref> (discrimination of pitch was relatively preserved in one of these cases<ref name=":7" />). In contrast, to patients with pure word deafness and general auditory agnosia, patients with non-verbal auditory agnosia were reported impaired at discriminating long gaps between click sounds, but impaired at short gaps.<ref name=":8">{{cite journal | vauthors = Motomura N, Yamadori A, Mori E, Tamaru F | title = Auditory agnosia. Analysis of a case with bilateral subcortical lesions | journal = Brain | volume = 109 ( Pt 3) | issue = 3 | pages = 379–91 | date = June 1986 | pmid = 3719283 | doi = 10.1093/brain/109.3.379 }}</ref><ref>{{cite journal | vauthors = Lambert J, Eustache F, Lechevalier B, Rossa Y, Viader F | title = Auditory agnosia with relative sparing of speech perception | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 25 | issue = 1 | pages = 71–82 | date = March 1989 | pmid = 2707006 | doi = 10.1016/s0010-9452(89)80007-3 | s2cid = 4484014 | doi-access = free }}</ref> A possible neuroanatomical structure that relays longer sound duration was suggested by Tanaka et al.<ref name=":4" /> By comparing the lesions of two cortically deaf patients with the lesion of a word deafness patient, they proposed the existence of two thalamocortical pathways that inter-connect the MGN with the auditory cortex. They suggested that spoken words are relayed via a direct thalamocortical pathway that passes underneath the putamen, and that environmental sounds are relayed via a separate thalamocortical pathway that passes above the putamen near the parietal white matter.

=== Amusia ===
Auditory agnosia patients are often impaired in the discrimination of all sounds, including music. However, in two such patients music perception was spared<ref name=":8" /><ref>{{cite journal | vauthors = Godefroy O, Leys D, Furby A, De Reuck J, Daems C, Rondepierre P, Debachy B, Deleume JF, Desaulty A | title = Psychoacoustical deficits related to bilateral subcortical hemorrhages. A case with apperceptive auditory agnosia | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 31 | issue = 1 | pages = 149–59 | date = March 1995 | pmid = 7781312 | doi = 10.1016/s0010-9452(13)80113-x | s2cid = 4481214 }}</ref> and in one patient music perception was enhanced.<ref>{{cite journal | vauthors = Mendez MF | title = Generalized auditory agnosia with spared music recognition in a left-hander. Analysis of a case with a right temporal stroke | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 37 | issue = 1 | pages = 139–50 | date = February 2001 | pmid = 11292159 | doi = 10.1016/s0010-9452(08)70563-x | s2cid = 14398211 }}</ref> The medical literature reports of 33 patients diagnosed with an exclusive deficit for the discrimination and recognition of musical segments<ref name=":0" /> (i.e., amusia). The damage in all these cases was localized to the right hemisphere or was bilateral. (with the exception of one case.<ref>{{cite journal | vauthors = Piccirilli M, Sciarma T, Luzzi S | title = Modularity of music: evidence from a case of pure amusia | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 69 | issue = 4 | pages = 541–5 | date = October 2000 | pmid = 10990522 | pmc = 1737150 | doi = 10.1136/jnnp.69.4.541 }}</ref>) The damage in these cases tended to focus around the temporal pole. Consistently, removal of the anterior temporal lobe was also associated with loss of music perception,<ref>{{cite journal | vauthors = Liégeois-Chauvel C, Peretz I, Babaï M, Laguitton V, Chauvel P | title = Contribution of different cortical areas in the temporal lobes to music processing | journal = Brain | volume = 121 ( Pt 10) | issue = 10 | pages = 1853–67 | date = October 1998 | pmid = 9798742 | doi = 10.1093/brain/121.10.1853 | doi-access = free }}</ref> and recordings directly from the anterior auditory cortex revealed that in both hemispheres, music is perceived medially to speech.<ref>{{cite journal | vauthors = Lachaux JP, Jerbi K, Bertrand O, Minotti L, Hoffmann D, Schoendorff B, Kahane P | title = A blueprint for real-time functional mapping via human intracranial recordings | journal = PLOS ONE | volume = 2 | issue = 10 | pages = e1094 | date = October 2007 | pmid = 17971857 | pmc = 2040217 | doi = 10.1371/journal.pone.0001094 | bibcode = 2007PLoSO...2.1094L | doi-access = free }}</ref> These findings therefore imply that the loss of music perception in auditory agnosia is because of damage to the medial anterior STG. In contrast to the association of amusia specific to recognition of melodies (amelodia) with the temporal pole, posterior STG damage was associated with loss of rhythm perception (arryhthmia).<ref>{{cite journal | vauthors = Di Pietro M, Laganaro M, Leemann B, Schnider A | title = Receptive amusia: temporal auditory processing deficit in a professional musician following a left temporo-parietal lesion | journal = Neuropsychologia | volume = 42 | issue = 7 | pages = 868–77 | date = January 2004 | pmid = 14998702 | doi = 10.1016/j.neuropsychologia.2003.12.004 | s2cid = 18348937 }}</ref><ref>{{cite journal | vauthors = Griffiths TD, Rees A, Witton C, Cross PM, Shakir RA, Green GG | title = Spatial and temporal auditory processing deficits following right hemisphere infarction. A psychophysical study | journal = Brain | volume = 120 ( Pt 5) | issue = 5 | pages = 785–94 | date = May 1997 | pmid = 9183249 | doi = 10.1093/brain/120.5.785 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Mavlov L | title = Amusia due to rhythm agnosia in a musician with left hemisphere damage: a non-auditory supramodal defect | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 16 | issue = 2 | pages = 331–8 | date = August 1980 | pmid = 7471774 | doi = 10.1016/s0010-9452(80)80070-0 | s2cid = 4487375 | doi-access = free }}</ref> Conversely, in two patients rhythm perception was intact, while recognition/discrimination of musical segments was impaired.<ref>{{cite journal | vauthors = Fries W, Swihart AA | title = Disturbance of rhythm sense following right hemisphere damage | journal = Neuropsychologia | volume = 28 | issue = 12 | pages = 1317–23 | date = January 1990 | pmid = 2280838 | doi = 10.1016/0028-3932(90)90047-r | s2cid = 28075918 }}</ref><ref>{{cite journal | vauthors = Murayama J, Kashiwagi T, Kashiwagi A, Mimura M | title = Impaired pitch production and preserved rhythm production in a right brain-damaged patient with amusia | journal = Brain and Cognition | volume = 56 | issue = 1 | pages = 36–42 | date = October 2004 | pmid = 15380874 | doi = 10.1016/j.bandc.2004.05.004 | s2cid = 33074495 }}</ref> Amusia also dissociates in regard to enjoyment from music. In two reports,<ref>{{Cite journal | vauthors = Lechevalier B | title = La querelle de l'aphasie | journal = Revue Neurologique | date = February 2017 | volume = 173 | pages = S10–1 | doi = 10.1016/j.neurol.2016.12.011 }}</ref><ref>{{cite journal | vauthors = Zhang Q, Kaga K, Hayashi A | title = Auditory agnosia due to long-term severe hydrocephalus caused by spina bifida - specific auditory pathway versus nonspecific auditory pathway | journal = Acta Oto-Laryngologica | volume = 131 | issue = 7 | pages = 787–92 | date = July 2011 | pmid = 21413843 | doi = 10.3109/00016489.2011.553631 | s2cid = 28225991 }}</ref> amusic patients, who weren't able to distinguish musical instruments, reported that they still enjoy listening to music. On the other hand, a patient with left hemispheric damage in the amygdala was reported to perceive, but not enjoy, music.<ref name="pmid14742630">{{cite journal | vauthors = Griffiths TD, Warren JD, Dean JL, Howard D | title = "When the feeling's gone": a selective loss of musical emotion | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 75 | issue = 2 | pages = 344–5 | date = February 2004 | pmid = 14742630 | pmc = 1738902 | doi = 10.1136/jnnp.2003.015586 }}</ref>

=== Word meaning deafness / associative auditory agnosia ===
In 1928, Kleist<ref name=":12" /> suggested that the etiology of word deafness could be due either to impaired perception of the sound (apperceptive auditory agnosia), or to impaired extraction of meaning from a sound (associative auditory agnosia). This hypothesis was first tested by Vignolo et al<ref>{{cite book |last=Vignolo|first=Luigi A. | name-list-style = vanc |chapter=Auditory Agnosia: A Review and Report of Recent Evidence |title=Brain & Behavior|date=2017-07-12|pages=172–208|publisher=Routledge|isbn=978-1-315-08203-5|doi=10.4324/9781315082035-8}}</ref> (1969), who examined unilateral stroke patients. They reported that patients with left hemisphere damage were impaired in matching environmental sounds with their corresponding pictures, whereas patients with right hemisphere damage were impaired in the discrimination of meaningless noise segments. The researchers then concluded that left hemispheric damage results in associative auditory agnosia, and right hemisphere damage results in apperceptive auditory agnosia. Although the conclusion reached by this study could be considered over-reaching, associative auditory agnosia could correspond with the disorder word meaning deafness.

Patients with word meaning deafness are characterized by impaired speech recognition but intact repetition of speech and left hemisphere damage.<ref name=":13">{{cite journal | vauthors = Bormann T, Weiller C | title = "Are there lexicons?" A study of lexical and semantic processing in word-meaning deafness suggests "yes" | journal = Cortex | volume = 48 | issue = 3 | pages = 294–307 | date = March 2012 | pmid = 21752361 | doi = 10.1016/j.cortex.2011.06.003 | s2cid = 24076165 }}</ref><ref name=":14">{{Cite journal| vauthors = Ellis AW | date = April 1984 |title=Introduction to Byrom Bramwell's (1897) case of word meaning deafness |journal=Cognitive Neuropsychology |volume=1 |issue=3 |pages=245–258 |doi=10.1080/02643298408252025 }}</ref><ref>{{cite journal | vauthors = Franklin S, Howard D, Patterson K | title = Abstract word meaning deafness | journal = Cognitive Neuropsychology | date = February 1994 | volume = 11 | issue = 1 | pages = 1–34 |doi=10.1080/02643299408251964 }}</ref><ref>{{Cite journal| vauthors = Franklin S, Turner J, Ralph MA, Morris J, Bailey PJ | title = A distinctive case of word meaning deafness? | journal = Cognitive Neuropsychology | date = December 1996 | volume = 13 | issue = 8 | pages = 1139–62 | doi = 10.1080/026432996381683 | url = https://www.research.manchester.ac.uk/portal/en/publications/a-distinctive-case-of-word-meaning-deafness(900feb4a-cb6a-4c5b-a26a-c67393c710d5).html }}</ref><ref>{{Cite journal | vauthors = Hall DA, Riddoch MJ | title = Word meaning deafness: Spelling words that are not understood. | journal = Cognitive Neuropsychology | date = December 1997 | volume = 14 | issue = 8 | pages = 1131–64 | doi = 10.1080/026432997381295 }}</ref><ref name=":12" /><ref name=":15">{{Cite journal | vauthors = Kohn SE, Friedman RB | title = Word-meaning deafness: A phonological-semantic dissociation. | journal = Cognitive Neuropsychology | date = August 1986 | volume = 3 | issue = 3 | pages = 291–308 | doi= 10.1080/02643298608253361 }}</ref><ref name=":16">{{Cite journal| vauthors = Symonds SC |date=1953-02-01|title=APHASIA|journal=Journal of Neurology, Neurosurgery & Psychiatry|volume=16|issue=1|pages=1–6|doi=10.1136/jnnp.16.1.1 |pmid=13023433|pmc=503107}}</ref> These patients often repeat words in an attempt to extract its meaning (e.g., "Jar....Jar....what is a jar?"<ref name=":13" />). In the first documented case,<ref name=":14" /> Bramwell (1897 - translated by Ellis, 1984) reported a patient, who in order to comprehend speech wrote what she heard and then read her own handwriting. Kohn and Friedman,<ref name=":15" /> and Symonds<ref name=":16" /> also reported word meaning deafness patients who are able to write to dictation. In at least 12 cases, patients with symptoms that correspond with word meaning deafness were diagnosed as auditory agnosia.<ref name=":0" /> Unlike most auditory agnosia patients, word meaning deafness patients are not impaired at discriminating gaps of click sounds.<ref>{{Cite journal| vauthors = Best W, Howard D | title = Word sound deafness resolved? | journal = Aphasiology | date = May 1994 | volume = 8 | issue = 3 | pages = 223–56 | doi = 10.1080/02687039408248655 }}</ref><ref>{{cite journal | vauthors = Slevc LR, Martin RC, Hamilton AC, Joanisse MF | title = Speech perception, rapid temporal processing, and the left hemisphere: a case study of unilateral pure word deafness | journal = Neuropsychologia | volume = 49 | issue = 2 | pages = 216–30 | date = January 2011 | pmid = 21093464 | pmc = 3031136 | doi = 10.1016/j.neuropsychologia.2010.11.009 }}</ref><ref>{{cite journal | vauthors = Nakakoshi S, Kashino M, Mizobuchi A, Fukada Y, Katori H | title = Disorder in sequential speech perception: a case study on pure word deafness | journal = Brain and Language | volume = 76 | issue = 2 | pages = 119–29 | date = February 2001 | pmid = 11254253 | doi = 10.1006/brln.2000.2417 | s2cid = 28958236 }}</ref> It is yet unclear whether word meaning deafness is also synonymous with the disorder deep dysphasia, in which patients cannot repeat nonsense words and produce [[semantic paraphasia]] during repetition of real words.<ref>{{cite journal | vauthors = Michel F, Andreewsky E | title = Deep dysphasia: an analog of deep dyslexia in the auditory modality | journal = Brain and Language | volume = 18 | issue = 2 | pages = 212–23 | date = March 1983 | pmid = 6188511 | doi = 10.1016/0093-934x(83)90016-0 | s2cid = 41300060 }}</ref><ref>{{cite journal | vauthors = Duhamel JR, Poncet M | title = Deep dysphasia in a case of phonemic deafness: role of the right hemisphere in auditory language comprehension | journal = Neuropsychologia | volume = 24 | issue = 6 | pages = 769–79 | date = January 1986 | pmid = 3808285 | doi = 10.1016/0028-3932(86)90076-x | s2cid = 25905211 }}</ref> Word meaning deafness is also often confused with [[transcortical sensory aphasia]], but such patients differ from the latter by their ability to express themselves appropriately orally or in writing.

== Neurological mechanism ==
Auditory agnosia (with the exception of non-verbal auditory agnosia and amusia) is strongly dependent on damage to both hemispheres.<ref name=":0" /> The order of hemispheric damage is irrelevant to manifestation of symptoms, and years could take between the damage of the first hemisphere and the second hemisphere (after which the symptoms suddenly emerge).<ref name=":10" /><ref name=":5" /> A study<ref>{{cite journal | vauthors = Griffiths TD, Johnsrude I, Dean JL, Green GG | title = A common neural substrate for the analysis of pitch and duration pattern in segmented sound? | journal = NeuroReport | volume = 10 | issue = 18 | pages = 3825–30 | date = December 1999 | pmid = 10716217 | doi = 10.1097/00001756-199912160-00019 }}</ref> that compared lesion locations, reported that in all cases with bilateral hemispheric damage, at least in one side the lesion included Heschl's gyrus or its underlying white matter. A rare insight into the etiology of this disorder was reported in a study of an auditory agnosia patient with damage to the brainstem, instead of cortex.<ref name=":9" /> fMRI scanning of the patient revealed weak activation of the anterior Heschl's gyrus (area R) and anterior superior temporal gyrus. These brain areas are part of the auditory 'what' pathway, and are known from both human and monkey research to participate in the recognition of sounds.<ref>{{cite journal | vauthors = Poliva O | title = From where to what: a neuroanatomically based evolutionary model of the emergence of speech in humans | journal = F1000Research | volume = 4 | pages = 67 | date = 2017-09-20 | pmid = 28928931 | pmc = 5600004 | doi = 10.12688/f1000research.6175.3 | doi-access = free }}</ref>

== See also ==
* [[Amusia]]
* [[Aphasia]]
* [[Apraxia]]
* [[Auditory verbal agnosia]]

== References ==
{{Reflist|30em}}

== Further reading ==
* {{cite journal | vauthors = Polster MR, Rose SB | title = Disorders of auditory processing: evidence for modularity in audition | journal = Cortex; A Journal Devoted to the Study of the Nervous System and Behavior | volume = 34 | issue = 1 | pages = 47–65 | date = February 1998 | pmid = 9533993 | doi = 10.1016/S0010-9452(08)70736-6 | s2cid = 2717085 | url = http://www.cogsci.ucsd.edu/~coulson/CNL/aud-disorders.pdf }}

== External links ==
* [http://www.psychnet-uk.com/x_new_site/DSM_IV/agnosia.html Psychnet Definition]

[[Category:Agnosia]]
[[Category:Medical terminology]]

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